| Title: | ATP regulates sodium channel kinetics in pancreatic islet beta cells |
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| Authors: | ID Zou, Na (Author)
ID Rupnik, Marjan (Author) |
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| Files: |  http://link.springer.com/content/pdf/10.1007%2Fs00232-012-9506-7.pdf
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| Language: | English |
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| Work type: | Not categorized |
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| Typology: | 1.01 - Original Scientific Article |
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| Organization: | MF - Faculty of Medicine
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| Abstract: | Pancreatic beta cells act as glucose sensors, in which intracellular ATP ([ATP](i)) are altered with glucose concentration change. The characterization of voltage-gated sodium channels under different [ATP](i) remains unclear. Here, we demonstrated that increasing [ATP](i) within a certain range of concentrations (2-8 mM) significantly enhanced the voltage-gated sodium channel currents, compared with 2 mM cytosolic ATP. This enhancement was attenuated by even high intracellular ATP (12 mM). Furthermore, elevated ATP modulated the sodium channel kinetics in a dose-dependent manner. Increased [ATP](i) shifted both the current-voltage curve and the voltage-dependent inactivation curve of sodium channel to the right. Finally, the sodium channel recovery from inactivation was significantly faster when the intracellular ATP level was increased, especially in 8 mM [ATP](i), which is an attainable concentration by the high glucose stimulation. In summary, our data suggested that elevated cytosolic ATP enhanced the activity of Na(+) channels, which may play essential roles in modulating cell excitability and insulin release when blood glucose concentration increases. |
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| Keywords: | Langerhansovi otočki, trebušna slinavka |
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| Year of publishing: | 2013 |
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| Number of pages: | str. 101-107 |
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| Numbering: | Vol. 246, iss. 2 |
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| PID: | 20.500.12556/DKUM-50505  |
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| UDC: | 612.349.7 |
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| ISSN on article: | 0022-2631 |
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| COBISS.SI-ID: | 512288568 |
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| NUK URN: | URN:SI:UM:DK:8YJ0HDMY |
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| Publication date in DKUM: | 10.07.2015 |
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| Views: | 2518 |
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| Downloads: | 283 |
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| Metadata: |    |
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| Categories: | Misc.
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